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Zika Virus Persistently and Productively Infects Primary Adult Sensory Neurons In Vitro

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dc.contributor.authorSwartwout, Brianna K.en
dc.contributor.authorZlotnick, Marta G.en
dc.contributor.authorSaver, Ashley E.en
dc.contributor.authorMcKenna, Caroline M.en
dc.contributor.authorBertke, Andrea S.en
dc.contributor.departmentPopulation Health Sciencesen
dc.contributor.departmentFralin Biomedical Research Instituteen
dc.contributor.departmentSchool of Neuroscienceen
dc.contributor.departmentVirginia-Maryland College of Veterinary Medicineen
dc.date.accessioned2018-02-01T13:40:04Zen
dc.date.available2018-02-01T13:40:04Zen
dc.date.issued2017-10-13en
dc.description.abstractZika virus (ZIKV) has recently surged in human populations, causing an increase in congenital and Guillain-Barré syndromes. While sexual transmission and presence of ZIKV in urine, semen, vaginal secretions, and saliva have been established, the origin of persistent virus shedding into biological secretions is not clear. Using a primary adult murine neuronal culture model, we have determined that ZIKV persistently and productively infects sensory neurons of the trigeminal and dorsal root ganglia, which innervate glands and mucosa of the face and the genitourinary tract, respectively, without apparent injury. Autonomic neurons that innervate these regions are not permissive for infection. However, productive ZIKV infection of satellite glial cells that surround and support sensory and autonomic neurons in peripheral ganglia results in their destruction. Persistent infection of sensory neurons, without affecting their viability, provides a potential reservoir for viral shedding in biological secretions for extended periods of time after infection. Furthermore, viral destruction of satellite glial cells may contribute to the development of Guillain-Barré Syndrome via an alternative mechanism to the established autoimmune response.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationSwartwout, B.K.; Zlotnick, M.G.; Saver, A.E.; McKenna, C.M.; Bertke, A.S. Zika Virus Persistently and Productively Infects Primary Adult Sensory Neurons In Vitro. Pathogens 2017, 6, 49.en
dc.identifier.doihttps://doi.org/10.3390/pathogens6040049en
dc.identifier.issn2076-0817en
dc.identifier.issue4en
dc.identifier.orcidBertke, AS [0000-0002-8941-8010]en
dc.identifier.urihttp://hdl.handle.net/10919/81981en
dc.identifier.volume6en
dc.language.isoenen
dc.publisherMDPIen
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/29027940en
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectGuillain-Barréen
dc.subjectZika virusen
dc.subjectautonomicen
dc.subjectneuronsen
dc.subjectsatellite glial cellsen
dc.subjectsensoryen
dc.titleZika Virus Persistently and Productively Infects Primary Adult Sensory Neurons In Vitroen
dc.title.serialPathogensen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherJournal Articleen
dcterms.dateAccepted2017-10-10en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/University Research Institutesen
pubs.organisational-group/Virginia Tech/University Research Institutes/Fralin Life Sciencesen
pubs.organisational-group/Virginia Tech/University Research Institutes/Fralin Life Sciences/Fralin Affiliated Facultyen
pubs.organisational-group/Virginia Tech/Veterinary Medicineen
pubs.organisational-group/Virginia Tech/Veterinary Medicine/CVM T&R Facultyen
pubs.organisational-group/Virginia Tech/Veterinary Medicine/Population Health Sciencesen

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